1.11 Drugs and the Peripheral NS Flashcards

1
Q

How does the PNS breakdown?

A

PNS to motor and sensory NS
Motor to somatic and autonomic
autonomic to sympathetic and parasympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which NS uses:

1) efferent nn fibres
2) afferent nn fibres

A

1) Sensory

2) motor`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which break down of motor NS is

1) voluntary
2) involuntary

A

1) somatic

2) autonomic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What happens to the following in

1) sympathetic innervation
2) parasympathetic innervation
a) pupils
b) lens of eye adjusts for ___ vision

A

1) Pupils dilate (peripheral vision)
b) far
2) Pupils constrict
b) closer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens to the following in

1) sympathetic innervation
2) parasympathetic innervation
a) HR
b) Blood vessels to limbs
c) to visceral organs
d) brain activity

A
1) Heart rate increases
Blood vessels to limb muscles dilate
Blood vessels to visceral organs constrict
Brain activity general alertness
2) Heart rate decrease
Blood vessels to limb muscles constrict
Blood vessels to visceral organs more dilated
Brain activity normalise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What happens to the following in

1) sympathetic innervation
2) parasympathetic innervation
a) Respiratory rate
b) salivary secretions

A

1) a) increases
b) reduced
2) a) decreases
b) increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

a) What neurotransmittor is used at the following junctions in sympathetic NS
1) preganglionic
2) postganglionic
b) What are the exceptions to this rile

A

a) 1) ACh (acetyl choline)
2) NA (noradrenaline)
b) sweat glands everything is ACh and , adrenal medulla, ACh causes secretionb of adrenaline into the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

a) What neurotransmittor is used at the following junctions in parasympathetic NS
1) preganglionic
2) postganglionic
b) At neuromuscular junctions in somatic what neurotransmittor is used

A

a) 1) ACh
2) ACh
b) ACh!!
(acetyl choline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe synthesis of Acetyl choline at junctions:

i.e. enzyme and substrates

A

choline/choline acetyl transferase (CAT) is the synthetic anexyme, formed from choline and AcCoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe storage of Acetyl choline at junctions:

2) WhY?

A

vesicles

2) prevent degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe release of Acetyl choline at junctions:

A

exocytosis into synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe receptor interactions of Acetyl choline at junctions:

A

binds to a muscarinic or a nicotinic receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe termination of Acetyl choline at junctions:

A

broken down in synapse by acetylcholine esterase (degradation enzyme)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The actions of ACh are mediated via 2 main classes of ACh receptor
Names:

A

Muscarinic receptors

Nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

1) What are the subclasses of muscarinic receptor?
2) What type of receptor is it ?
3) Where is the receptor located within the body?
4) response time compared to nicotinic?

A

1) M1,2,3,
2) G protein coupled
3) Located at postganglionic parasympathetic synapses
(found at target organ/ effector tissue)
4) slow (seconds)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nicotinic receptors (nACh), What are the 2 main receptor subtypes: (excitatory? or inhibitory?)

b) what type of receptor is it?
c) Where is it located?
d) response time compated to muscarinic:

A

muscle-type: neuromuscular junction (NMJ) (excitatory)

2) neuronal type- brain and autonomic ganglia (excitatory)
b) Ligand gated ion channels (or ionotropic receptor)
c) Located in ganglia and on NMJ ( preganglionic and in muscles(“only” target mm found in))

17
Q

Fill spaces:
• Muscarinic receptors are just located in A.
• Nicotinic neuronal type are involved in B
• Nicotinic muscle type are involved in C

A

A) parasympathetic system,
B) parasympathetic and sympathetic system.
C) somatic effects.

18
Q

Knowing muscarinic receptors are involved in the parasympathetic system. What effect does a muscarinic A)agonist and B) antagonist have on:

1) pupillary muscle in pupil
2) focal length of lens (ciliary mm)
3) bronchioles

A

A) 1) increases pupil constriction (contraction)
2) decreases focal length (contracts)
3)Bronchoconstriction
B) the opposite

19
Q

Knowing muscarinic receptors are involved in the parasympathetic system. What effect does a muscarinic A)agonist and B) antagonist have on:
1) cardiac output (=HR*SV(force))
2) GI motility
3) exocrine gland secretion (sweating, salivation, bronchiol secretion)
C) Whats wrong with this?

A
A)1) decrease
2) increases
3) increases
B) the opposite 
C) sweating is actually a sympathetic effect
20
Q

1) What are muscarinic agonists know as ?
2) Why?
3) What are muscarinic antagonists known as ?

A

1) as parasympathomimetics
2) they stimulate muscarinic receptors
3) as parasympatholytic .

21
Q

Considering the effects of antagonist muscarinic receptors what are they used for get a few:

A

pupil dilation in eye surgery , decrease oral /respiratory secretions before oral procedures and as an adjunct to anaesthesia (as when your on ventilator you don’t have cough reflex), resuscitation in bradycardia, asthma patients , GI motility= motion sickness

22
Q

Considering the effects of agonist muscarinic receptors what are they used for get a few:

1) how does it treat glaucoma (build of lfui din the eye)
2) the oral condition it treats
a) how is it taken
b) side effects

A

1) focus on near vision + also allows increase drainage of aqueous humour
Contraction of sphincter muscle causes pupil constriction
2) xerostomia: stimulates saliva secretions
a) Taken systemically
b) Side effects: muscarinic-sweating, nausea, minimal cardiovascascular side effect (due to low dose)

23
Q

Treatment for :

1) asthma
2) Xerostomia
3) Motion sickness (decrease gastric motility)
4) Bradycardia

A

muscarinic antagonist: 1,3, 4

muscarinic agonist: 2

24
Q

Treatment for :

1) to decrease secretions
2) pupil dilation in eye surgery
3) glaucoma

A

muscarinic antagonist: 1,2,

muscarinic agonist: 3

25
Q

What is the effect of nicotinic antagonists?

A

loss of sympathetic & parasympathetic reflexes, especially cardiac

26
Q

What is the effect of nicotinic agonists targeting nicotinic receptors found at NMJ?

2) What is the importance of this in medicine when agonist is SYNTHETIC:
3) What does it cause?
4) used when?

A

Stimulation of these receptors by ACh causes depolarisation (in muscle fibre this is known as an end plate potential (EPP)) and contraction of the skeletal muscle fibre

2) Because the synthetic agonist is not metabolised rapidly by acetylcholinesterase, the fibre is persistently depolarised resulting in loss of further electrical excitability-known as depolarising block
3) depolarising block
4) paralysis/ muscle relaxation (for surgery)

27
Q

nicotinic agonists or antagonstic cause :

1) depolarising block
2) non-depolarising block
b) why?
c) What do they both have in common?

A

1) agonist b)synthetic agonist is not metabolised rapidly by acetylcholinesterase,fibre is persistently depolarised resulting in loss of further electrical excitability-known as depolarising block
2) antagonist b) Hyperpolarisation, inhibition of EPPs (initial depolarisation)
Muscle fibre relaxation
c) both cause paralysis (used in surgery)

28
Q

What is anticholinesterases used to for? (2)

A

Myasthenia gravis

Induce paralysis for surgery

29
Q

what is used to treat myasthenia gravis?

2) how does it work?
3) What is this disease?

A

1) anticholinesterases
2) inhibits acetylcholinesterase, thus ACh not metabolised nad action not terminated, amount of ACh isecreted increase therefore can have greater effect. Too much and can be harmful
3) (autoimmune disease, circulating antibodies against muscle nicotinic receptors)